4.5 Article

Developmental and injury-induced expression of α1β1 and α6β1 integrins in the rat spinal cord

期刊

BRAIN RESEARCH
卷 1130, 期 1, 页码 54-66

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.brainres.2006.10.072

关键词

angiogenesis; blood vessel; oligodendrocyte precursor; preganglionic neuron; spinal cord injury

资金

  1. NCRR NIH HHS [RR15576, P20 RR015576] Funding Source: Medline
  2. NINDS NIH HHS [R01 NS045734] Funding Source: Medline

向作者/读者索取更多资源

Loss and damage to blood vessels are thought to contribute to secondary tissue loss after spinal cord injury. Integrins might be therapeutic targets to protect the vasculature and/or promote angiogenesis, as their activation can promote tubule formation and survival of endothelial cells in vitro. Here, we show that immunostaining with an antibody against the alpha(1)beta(1) integrin heterodimer is present only in blood vessels from postnatal day 1 (P1) through adulthood in Sprague-Dawley rats. After a spinal cord contusion at T9 in adults, the area of alpha(1)beta(1) integrin positive blood vessels increases within 11 mm from the injury site at 3 days post-injury and remains prominent within the injured core only at 7 days. Staining for the alpha 6 beta 1 integrin heterodimer increases in blood vessels between P10 and adulthood and is present in preganglionic neurons of the intermediolateral cell column (IML) at all ages. The alpha 6 beta 1 integrin is also expressed by motor neurons postnatally, and oligodendrocyte precursors (OPCs), as previously reported. After the contusion, the area of alpha 6 beta 1-stained blood vessels is increased at 3 days and most prominently, 1 mm from the injury site, followed by a significant reduction at 7 days, when alpha 6 beta 1 integrin staining is most prominent around the injured core. Staining is also present in a subset of microglia and/or macrophages. These results raise the possibility that alpha(1)beta(1) and alpha(6)beta(1) integrins in blood vessels might be targeted to reduce blood vessel loss and promote angiogenesis, which may promote tissue sparing after spinal cord injury. (c) 2006 Elsevier B.V. All rights reserved.

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